I’ve recently become highly politicized over rights abuses and intolerable corporate stature in my country. I have privately — and quietly — become convinced that the US healthcare system is so completely predatory, so opposed to its own mandate, that it will never offer healing for anyone in my position.

Debbie’s death has broken through my professional anxiety about appearing detached and scientifically sound. I have, at long last, become politicized about the most important subject in my life, after 25 years of personal and professional involvement up to my back teeth.

I have minimized my discussion here of what actually works. That dishonest omission has done us all a great disservice. I’m going to discuss what works, whether or not it’s FDA approved, pharmaceutically profitable, or adequately studied.

Medical studies are a shining example of the fact that we inspect what we expect, not necessarily what we need. The fact that studies have not been done on most modalities, or not rigorously done in double-blind experiments, doesn’t mean the modalities don’t work.

It means the studies need to be done. Period.

Where I understand the mechanisms of action, I will explain them. Where studies don’t exist, I’ll detail what should probably be explored.

But I have had enough of silence. I will not die as Debbie did. I will not die on the table. I certainly will not die saturated with soul-destroying pharmaceutical-grade poisons, as so many of us do.

I will find a better way. I will find a way that works. I’ll do my best to persuade others to study the modalities involved, and to fund the studies. My legislators will learn to recognize my name on sight, because their slavish debt to the pharmaceutical industry is absolutely intolerable and it’s up to me, and others like me, to convince them of that.

I wish Debbie a painless and peaceful rest. I hope her extraordinary husband finds enough strength and comfort to manage life without her.

For myself, I want the intelligence, resources and strength to find a solid cure, make it happen, and spread the word.

“Standard” treatments don’t work well for me; moreover, they involve invasive procedures too brutal to tolerate and medications I’m either outright allergic to, or that impair me so profoundly I can no longer function. At all.

So I took myself off my meds, thought things over, and came to the following conclusions.

MY CHRONIC PAIN MANIFESTO

Yes, it hurts.It’s going to anyway.

So should I hoard my daysAnd fast from life?Comfort myself with poisons,Blister-packed and FDA approved?

Some think it would be best all ’round.I’d cure them if I could (heh!)But I’m too tired forYet another pointless struggle.

The sunlight pours through trees like proseccoAnd reminds me what it means to live:

Voices warm with love, theMouth-smack of good food,The hug of hills and theRough snuggles of the sea.

Feast on this: The cost of life is much the same. The difference lies in how you spend it.

How is this relevant to medical science? For one thing, it shows just how badly off base it is in vivo. Like any manifesto, it makes an explicit declaration: fundamental attitudes must change.

Policy determines what will be profitable, and profit opportunities determine what science gets funded. There is no profit in fully-functioning people, but there’s plenty in people who are too sick to function but not sick enough to die … for awhile.

Policy could allow my insurance to cover the things that do work (massage, reiki, homeopathy, yoga), especially given the detailed and vivid documentation I’ve provided of just how well they work. Nobody will fund science studies on these in any volume, because it is so much more profitable to drug people into silence.

There are vague mentions in the literature of myelination in CRPS, but researchers are so busy trying to figure out how to pill CRPS — a highly pillable disease — that such mechanistic issues get surprisingly little play.

Myelin is the protective sheath of fat that keeps your neurons safe and warm, so they can do their work. Without myelin, your nerves can’t fire properly — or else they can’t stop firing. They need the myelin sheath. Little kids need to take in a certain amount of cholesterol so their growing bodies can build good myelination. Demyelination, that is, the loss of that sheath, is most famously known for its role in Lou Gherig’s disease.

I’ve long suspected that demyelination is both an important sign of disease progress and a powerful contributing factor to further degeneration of the peripheral, if not the central, nervous system in CRPS. However, there’s not much in the literature, probably because it’s a useless treatment marker in someone who’s beyond treatment.

This brings us to the particularly delightful issue of finding corpses to study, since until now we could only check myelination after autopsy, and those who donate their bodies to science are filed under what took their lives.

People with CRPS develop heart disease, cardiovascular disease, bleeding disorders, organ failure, vision impairment, and staggering depression as a direct consequence of CRPS. However, when they drop dead, get struck by a bus they couldn’t see, or take their own lives, we don’t say “They died of CRPS.” We say, “They died of heart disease, organ failure etc., traffic accident, or suicide” (– if we’re feeling kindly, “or depression.”)

Thus, there’s no way to identify the actual mortality rate of CRPS, although there unquestionably is one.

Diabetes, cancer, and AIDS get more dignity than this. I’d like to see our mortality rate properly attributed, not swept under the enormous rug of opportunistic conditions. This would contribute hugely to better medicine.

Doctors hate seeing patients hurt, but after awhile they can turn away from that, in order to drag themselves back to the office; they hate to see them die on their watch, and it makes them apply upward pressure on the reimbursement and legislative aspects of the care system.

There’s nothing like a mortality rate among those in their “productive years” to make legislators sit up and take notice.

I started nursing within a decade of the first AIDS diagnosis; my first job was on an AIDS unit. I’ve seen it work.

Let’s get our deaths properly attributed. It’s one last gift we can give our compatriots as we head out the door. I’m going to put it in my will.

Here’s what the jargon means.// ed. note: my comments and clarifications are picked out by those two slashes and the contraction for “editorial notation.”

One important factor in CRPS is inflammation that starts in the nerves. Microglia and astrocytes, which are the inflammatory and immune cells of the nervous system, get active enough to cause worse pain by themselves.

That’s a sparking astrocyte. Pretty, eh?

// ed. note: The inflammatory and immune responses are mixed blessings throughout the body. An immune response is uncomfortable; think about the last time you had the flu — sucked, huh? An inflammatory response can cause pain due solely to the inflammation, like with some kinds of arthritis. So, for the microglia and astrocytes to make pain worse is not a surprise, since that’s what immune response and inflammation can do anywhere.

One type of immune cells normally floating in your blood, called monocytes, can get into the brain and spinal cord and turn themselves into the nervous system’s immune cells, microglia. The added level of inflammatory/immune response leads to more pain.

// ed. note: Again, not as strange as it sounds. The body’s living cells all contain complete DNA, and they are designed to be both helpful and appropriate; heart cells transplanted into muscles become muscle cells, and muscle cells transplanted in the heart become very much like heart cells. So, for this type of small white blood cells to turn into microglia is reasonable.

These are microglia in various active states.

// ed. note: The inflammatory response releases cytokines. Cytokines are the chemical widgets, produced in inflammation, that serve as the chemical messengers running around the cells screaming that the sky is falling. Some cytokines increase inflammatory pain, some cytokines reduce it.

This study looked for particular kinds of inflammatory monocytes in the blood, to test the assumption that higher levels of these particular types of monocytes (which can then turn into microglia, making the inflammation and pain worse, etc.) are related specifically to CRPS.

Now here’s the fun part. The basic blood-borne indicators of inflammation and illness were no different in those with CRPS than in normal people. That’s why conventional lab results, like “complete” blood counts, come back normal for us. However, the proportion of the particular types of monocytes associated with CRPS, were significantly higher in those with CRPS. The type of cytokine that reduces inflammatory pain, was also significantly lower in people with CRPS.

That means the inflammatory process screws us coming and going, and screws specifically us, the people with CRPS, in ways that can be checked in a lab.

OK, GTK.

These are sensible scientists: they state that they don’t know if the monocyte proportions changed before or after the onset of CRPS, or both before and after. If before, it might indicate a predisposition to CRPS, in which case surgeries and accidents have to be handled with specific care for antioxidant therapy and aggressive pain control. If after, it might be relevant in figuring out how things are going and if what the doc is doing works.

Also, some drug company could make a staggering fortune off of new meds that mess with this process. They actually mention that at the end of the article, which means someone has to fund their work.

// ed. note: Be fair. We have a profit-based health care system driven by enormous corporations that are traded on the stock exchange, and the Sarbanes-Oxley laws mean that their first obligation is to their shareholders. Not patients. Not customers. But shareholders.

Conventional medicine has to come back to profitability. There are more direct ways to address these immune and inflammatory issues by existing means, which could be further developed, but they don’t sustain the pharma industry’s usual annual returns of 20-40% — a rate of stock profitability matched only by oil companies.

Glial cells are part of the nervous system, kind of woven throughout it, appearing more densely in some areas (the brain) than others (the fingertips.) They were formerly considered to be just support structures, but I remember, back around 1990, reading articles linking them to inflammatory processes in the brain. Therefore I figured they were part of the brain’s immune system, but science (and funding) didn’t make that short leap (inflammation to immune response) until recently. Now they’re considered key to the brain’s own immune system.

This is interesting because the circadian rhythm is disrupted in CRPS, and we’ve recently learned that astrocytes and other glial cells are disrupted by CRPS too. Assuming human’s astrocytes are functionally similar to fruit flies’ astrocytes, that circadian rhythm issue might be caused — or at least mediated — by those twinkling astrocytes.

Mitochondria (from the Greek, meaning “string grain” — yeah, it’s lame, but it sounds good in Greek) are independent little one-celled organisms that live inside your cells and make energy for them. If you ever studied the ATP cycle (also called the Krebbs cycle or the citric acid cycle, depending on where you went to school and how deeply they went into it), then you should know that this is where the ATP cycle takes place.

Without mitochondria, you have no way of converting food into energy.

When you were being conceived, half your cells’ genes came from your mother and half from your father. All of the other stuff that goes inside a cell came from your mother. This includes the mitochondria. (This is why mitochondrial DNA is used to track maternal inheritance: it always comes down the female line.) Your mother’s cell hosts conception, just as (normally) your mother’s body hosts gestation.

Mitochondria have a fairly smooth outer layer and a deeply-rumpled inner layer. Most of the action happens inside the rumpled layer. This is where the ribosomes, most of the fluids and loose protein, and the ATP-making particles hang out.

Cells, including mitochondria, need various proteins to do their work with. Large proteins get carefully handed from the outside world, through the outer layer of the mitochondrion (singular of “mitochondria” — sorry, it’s still Greek), then into the inner layer.

If the smooth outer layer is damaged, this makes this transfer process screw up, and the inner layer gets disrupted, ripping up the cell. Granules and nucleic acids all over the place. Bang goes that ATP production.

Knowing why it’s so damnably exhausting to walk a mile, when it used to be fun — fun! — to run 3, is a bit of a relief. First question that leaps to my mind: How do I fix ’em? How do I give them what they need to get better and protect themselves? The answer seems simple: antioxidants are what’s needed to prevent and repair that damage (good explanation of that here) to the walls of the mitochondrial cell. Mitochondria are both the biggest makers of reactive oxygen species and the biggest scavengers of them, so of course it makes sense that that’s exactly the kind of help they need when they can’t keep up.

Downing antioxidants by the bucketful is one way to get them in. Intriguing for three reasons:

Kind of depressing for one simple reason: it’s iffy whether, once you’ve got the disease process going, the antioxidants can get where they’re needed and save your poor beleaguered mitochondria. … Having said that, I notice that the writers of that article seem to be trying to sell something, and that makes me very suspicious of their conclusions.

Next, I’ll offer suggestions for patients, suggestions for clinicians, and then wind this up with a foray into the question of whether mitochondrial issues have a genetic component, like being X-linked — the way a cat’s fur color is!

For people with CRPS — So what is a poor, confused CRPSer to do?

Two things that you hardly need reminding of:

Trust your sense of your own body.

Do what works for you.

Most antioxidants are not going to hurt you, without letting you know first (that is, make you nauseous or feel funny.) Take vitamin C in doses no larger than 500mg, since larger doses tend to trigger your gut to throw the C away. Go ahead and try stress-vitamins, co-enzyme Q-10, N-acetylcysteine, hair-skin-&-nails vitamins (these are really fat-soluble antioxidants) … try things, take what helps, and put aside the rest if they don’t do anything. Keep in mind that things change: what doesn’t work now might work later, and vice-versa.

For antioxidant powerhouses, look for dark-red and dark-blue fruits: pomegranates, blueberries, red wine, chocolate (though some CRPS people have to avoid that for its nerve effects), mangosteen (my favorite fruit), cranberries, and so on.

Stay smart. Stay loose. Keep going.

For medical people — clinical takeaways:

Most treatment standards, particularly for CRPS, are based on science that’s over a decade old. They shouldn’t be changed blithely but they can certainly be improved. There is plenty of room for that.

The following points are intended as additions to the standards you follow for CRPS, as they are good guidelines for mitochondrial and neurologic support in a system compromised by CRPS.

After any limb surgery, give Vitamin C 500 mg, QD or BID, for a couple weeks beforehand and 30-50 days after — or to metabolic tolerance, if that’s too much. Use a food-associated form for best uptake. This one intervention will reduce the risk of developing CRPS by 80%, according to the best current data.

We assume your patients are taking an adequate multivitamin and are eating plenty of greens, dark fruits, and wholesome proteins. So make sure they are. Direct them to food bank, food stamps or other food assistance as needed. Give recipes. (No kidding.) 2 benefits: better antioxidant uptake if taken with antioxidant-rich food, and increasing the patient’s own sense of agency/participation improves pain and affect. (If you don’t believe in multivitamins, then get out of the supermarket/pharmacy and get some real ones.)

Give “uber-antioxidants” like ubiquinone (co-Q 10), N-acetylcysteine, or glutathione. There are indications that these can provide substantial benefit — though again, not normally curative of chronic CRPS. They are impressive, especially for mitochondrial-dysfunction issues.

These ranges are empirical; if you can find the funding to do the science to develop more reliable ranges for this population, so much the better.

Adequate tissue oxygenation and perfusion can return substantial function and significantly reduce pharmacologic burden. Patients can demonstrate this, even where the data have not been published and peer reviewed. Therefore, use antioxidants rigorously and intelligently.

Why all that anti-oxidation when the medical literature is not definitive? 2 reasons, which you ought to know for yourselves:

Between the cortisol and systemic oxidative stresses, it can’t hurt and it will help something. You’ll see a distinct improvement in affect, activity, motivation and well-being when the dose is optimized, even if it can’t be expected to be curative. Making your patient’s life more bearable is an essential part of your job.

Let’s say this together, everyone: statistics mean nothing in the case of the individual. Accepted, standardized medicine is what you start with, but, when your case is taking you out to the margins, you go to the margins, because that’s where your success is most likely to await.

Keep in mind that doctors are not the only scientists interested in the human body. Be prepared to look into other disciplines for leads when your own offers no good options.

The accepted style is very different, but the info they have is tremendous.

Forward-looking thoughts:

Consider infusing vitamin K into CRPS-damaged tissues. I would love to see studies on that.

Figure out how to deliver antioxidants in a targeted way. (Now! Please!) This would be a good way to save a lot of lives and end tons of misery.

… And for all curious people …

Let’s go back to mitochondria in reproduction. Kind of in an X-rated way, figuratively speaking.

We know that women have two X chromosomes. The Y chromosome is a stubby little object with hardly any data to use, unless you’re into color-blindness or hemophilia; this means women have quantities of extra data, which can have even more devastating effects (as in, Down syndrome.) So how to handle the extra genes?

Pick one. Simple as that.

Shortly after conception, when the cells are just dividing like mad and haven’t decided what to be yet, every single cell turns off one of its two X chromosomes; each of that cell’s daughter cells inactivates the same X chromosome. As the cells continue to multiply, then fill out, fold, bend around, and specialize, to become a whole, separate being, it means that X-linked traits appear in a mottled pattern throughout the body, as the two sets of daughter cells continue reproducing and passing on their particular X-activations. Isn’t that curious?

As an especially decorative instance, cats’ hair color is an X-linked trait:

Cool, huh? Love her accent, too.

But this fact brings me to a serious question about mitochondrial disease. If mitochondria are sex-linked, is there a relationship between the X chromosome and mitochondrial expression? It seems improbable that there wouldn’t be, because mitochondria reside inside the cell, and the cell’s action is determined by the genes within it. The mitochondria had to have developed a special relationship with the X’s in the 23rd chromosomal pair, after all those millenia.

It’s generally accepted that mitochondrial diseases are due to toxification or to complex, multigenetic issues. Ok, fine. But what about mitochondrial vulnerabilities that don’t become pathologic until they are damaged in some other way? To what degree is toxification an issue related to X-activation? In other words, is mitochnodrial vulnerability related to vulnerabilities in the active X chromosome?

Is there a patchy characteristic to the early stages of mitochondrial destruction? — You know, the early stages of rare disorders, the time when it’s impossible to get a diagnosis because the doctors are all so busy chasing their own tails around your irrational symptoms and their own ignorance.

Is that initial “mottled” activity one reason why these diseases are so damn weird?

I have CRPS-1/RSD/causalgia, and when your condition has more than one name, it’s a bad sign. I was a nurse, I was a tech writer, and I remain fascinated by health and technology.

Some parts of my brain have blown gaskets, but examining the science relating to neurology/immunology/endocrinology — and mulling how it could work in real life — seems to go just fine. It’s appropriate to both my professions that I want to track, document, and share what I learn.

You’re invited to watch and engage in this interesting journey. It’s taking place at an unimaginably rich, burgeoning age of technological development and biological understanding.